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机构地区:[1]西安医科大学病理解剖学教研室
出 处:《西安医科大学学报》1991年第4期333-337,共5页Journal of Xi'an Medical University(Chinese)
基 金:国家自然科学基金
摘 要:本文观察了27例癌性胸腹水中肿瘤相关性淋巴细胞(TAL)的白细胞间介素2(IL-2)产生能力并与结核患者进行了比较。结果发现TAL产生IL-2明显低于结核组;加入8%的肿瘤相关性巨噬细胞(TAM)可抑制TAL的IL-2产生而结核组中需加16%的巨噬细胞才有抑制作用;消炎痛可逆转这种抑制。TAL可抑制PBL对PHA刺激的增殖反应。作者认为癌性渗出浓淋巴细胞功能降低与抑制性淋巴细胞的存在及TAM抑制活性增强有关。TAM的抑制作用似主要通过释放PGE而实现。The ability of IL-2 production of tu-mor-associated lymphocytes(TAL)form effu-sions of 27 cancer patients were observed, using Iymphocytesfrom tuberculous effusions as control. We foundthat the ability of IL-2 production of TAL wassignificantly decreased as compared with that of tubercu-lous lymphocytes. When 8% tumor-associatedmacrophages (TAM) was added to the reactive sys-tem, the IL-2 production of TAL was markedlyinhibited However, in tuberculous group, 16% Mφwas needed to suppress the IL-2 production.Indomethacin could eliminate the suppressive functionof TAM. In addition, the TAL could inhibit theproliferation of autolougous PBL stimulated by PHA.These results suggest that the presence of suppressorlymphocyte among TAL and increased suppressive ac-tivity of TAM are mainly responsible for the decreasedeffective functions of TAL. Secretion of PGE probablyplays the chief role in the inhibitory activity of TAM.
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